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. 2021 Jan 23;23:11. doi: 10.1186/s13058-021-01391-1

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — Leronlimab blocks CCR5-mediated invasion of human breast cancer cells into the extracellular matrix. To test the ability of leronlimab to block cell invasion in 3D Matrigel invasion assay, MDA-MB-231 cells were used. CCL5 was used as chemoattractant to induce invasion. The small-molecule inhibitor of CCR5, vicriviroc, was used as a form of positive control. Leronlimab reduced CCL5-induced MDA-MB-231 breast cancer cell invasion with similar efficacy as vicriviroc (a, b) (855 ± 8.7, N = 8 for control vs. 520 ± 9.1, N = 9 for leronlimab, P < 0.001). We also tested the effects of leronlimab doses on breast cancer cell invasion, and the results showed that both 175 and 350 μg/ml of leronlimab can effectively block MDA-MB-231 cell invasion (c, d)